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Accessory Proteins for Melanocortin Signaling
Author(s) -
HE LIN,
ELDRIDGE ADAM G.,
JACKSON PETER K.,
GUNN TERESA M.,
BARSH GREGORY S.
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2003.tb03192.x
Subject(s) - ubiquitin ligase , transmembrane protein , melanocortin , melanocortin 1 receptor , gene , biology , neurodegeneration , microbiology and biotechnology , receptor , hair follicle , transmembrane domain , phenotype , genetics , ubiquitin , medicine , disease
A bstract : Switching from eumelanin to pheomelanin synthesis during hair growth is accomplished by transient synthesis of Agouti protein, an inverse agonist for the melanocortin‐1 receptor (Mc1r). The coat color mutations mahogany and mahoganoid prevent hair follicle melanocytes from responding to Agouti protein. The gene mutated in mahogany , which is also known as Attractin ( Atrn ), encodes a type I transmembrane protein that functions as an accessory receptor for Agouti protein. We have recently determined that the gene mutated in mahoganoid , which is also known as Mahogunin ( Mgrn1 ), encodes an E3 ubiquitin ligase. Like Attractin , Mahogunin is conserved in invertebrate genomes, and its absence causes a pleiotropic phenotype that includes spongiform neurodegeneration.